Both glycolysis and fatty acid oxidation become inhibited in ischemic tissue. The inhibition of glycolysis develops at the level of glyceraldehyde-3-phosphate dehydrogenase and is related to accumulation of hydrogen ion, NADH and lactate in the cytosolic space. Fatty acid utilization becomes inhibited at the level of beta-oxidation and is related to an accumulation of NADH in the mitochondria. The reversibility of these pathways upon restoration of coronary flow after various periods of ischemic perfusion will be tested. The rate of glycolysis will be maximally stimulated in control and ischemic hearts by perfusing under anoxic conditions. If the maximum rate of glycolysis is reduced as a result of ischemia, the specific activity of glycolytic enzymes will be determined in control and ischemic hearts. The rate of fatty acid oxidation will be stimulated by restoring coronary flow to normal and perfusing with oxygenated buffer containing uncouplers of oxidative phosphorylation. This should allow the rate of fatty acid oxidation to be maximally stimulated in both control and in hearts following various periods of ischemic perfusion. These studies should determine whether energy production in ischemic hearts is reduced only because of accumulation of metabolic products which inhibit these pathways or because of irreversible alteration of enzymes in the pathways.